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Kamikado, Chiaki, Toshishige Shibamoto, Minoru Hongo, and Shozo Koyama. Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers. Am J Physiol Heart Circ Physiol 286: H121-H130, 2004. First published August 28, 2003 10.1152/ajpheart.01136.2002We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance (R t) was assigned to the portal (R pv), sinusoidal (Rsinus), and hepatic venous (Rhv) resistances using the portal occlusion (P po) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. R pv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH 2O. As Hct increased at a given blood flow, all three segmental vascular resistances of R pv, Rsinus, and Rhv increased at flow Ͼ15 ml/min. As blood flow increased at a given Hct, only R sinus increased without changes in R pv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, R sinus, but it did not affect Rhv. Finally, we estimated P po and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that P po and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect R sinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. P po and Phvo can be obtained by the double occlusion method in isolated perfused rat livers. blood viscosity; hepatic circulation; hepatic vascular occlusion methods LIVER AND LUNG circulation is analogous (19). Both the pulmonary artery and the portal vein are unique in their ability to carry large flows of venous blood under low hydrostatic pressures. The pulmonary arterioles and the portal venules have a similar anatomy (19). The vascular arrangement of the hepatic units is analogous to that of the lung in that both lobules have a central inflow (pulmonary artery and portal vein) and a peripheral outflow (pulmonary vein and hepatic vein) (18). In addition, embryologically, the tracheo-bronchial tree and the biliary ductal system originate from the gut.The longitudinal distribution of pulmonary vascular resistance has been extensively studied using vascular occlusion techniques, and the pulmonary vasculature can be represented by a simple hydrodynamic model consisting of three segments in series, each with a characteristic resistance and compliance (10, 12). The middle segment, which contains the capillaries, has relatively low resistance and high compliance, and the other two segments have relatively low compliance and high resistance. The pulmonary arterial and venous occlusion technique (9-11) allows partitioning ...

The localization of increased intrahepatic vascular resistance and the segmental vascular responsiveness to endothelin-1 are not well known in liver cirrhosis. We determined the segmental vascular resistances and their response to endothelin-1 of isolated portally perfused bile duct ligation (BDL)-induced cirrhotic rat livers. The portal occlusion pressure (Ppo) and the hepatic venous occlusion pressure (Phvo) were obtained by analyzing the profiles of the portal (Ppv) and hepatic venous (Phv) pressures during the double occlusion maneuver of simultaneous occlusions of the inflow and outflow perfusion lines. From the pressure gradients among Ppv, Ppo, Phvo, and Phv, the portal-hepatic venous resistance was assigned to three segments of the portal [Rpv = (Ppv - Ppo)/blood flow (Q)], sinusoidal [Rsinus = (Ppo - Phvo)/Q] and hepatic venous [Rhv = (Phvo - Phv)/Q] resistances. Rsinus, but not Rpv or Rhv, was significantly greater in BDL livers than in sham livers. Endothelin-1 (0.1-1 nM) increased Rpv and Rsinus to a similar magnitude, but not Rhv, in both sham and BDL. At 3 nM, the responsiveness of Rpv was smaller in BDL than in sham, but that of Rsinus were similar between in BDL and sham. In conclusion, increased sinusoidal resistance accounts for increased intrahepatic resistance of BDL-induced liver cirrhosis. Endothelin-1 contracts portal veins and sinusoids, but not hepatic veins, in both sham and cirrhotic livers. Sinusoidal contractility to endothelin-1 is not impaired in cirrhotic livers.

Anaphylactic shock in rats is characterized by antigen-induced hepatic venoconstriction and the resultant portal hypertension. We determined the role of portal hypertension in anaphylactic hypotension by using the side-to-side portacaval shunt- and sham-operated rats sensitized with ovalbumin (1 mg). We measured the mean arterial blood pressure (MAP), portal venous pressure (PVP), and central venous pressure (CVP) under pentobarbital anesthesia and spontaneous breathing. Anaphylactic hypotension was induced by an intravenous injection of ovalbumin (0.6 mg). In sham rats, the antigen caused not only an increase in PVP from 11.3 cmH(2)O to the peak of 27.9 cmH(2)O but also a decrease in MAP from 103 mmHg to the lowest value of 41 mmHg. CVP also decreased significantly after the antigen. In the portacaval shunt rats, in response to the antigen, PVP increased slightly, but significantly, to the peak of 17.5 cmH(2)O, CVP did not decrease, and MAP decreased to a lesser degree with the lowest value being 60 mmHg. These results suggest that the portacaval shunt attenuated anaphylactic portal hypertension and venous return decrease, partially preventing anaphylactic hypotension. In conclusion, portal hypertension is involved in rat anaphylactic hypotension presumably via splanchnic congestion resulting in decreased venous return and thus systemic arterial hypotension.

Introduction: We describe a case of pulmonary gas embolism caused by portal vein gas (PVG) observed using echocardiography. Echography revealed gas flowing through the hepatic vein, inferior vena cava, right atrium, and right ventricle, as well as pulmonary hypertension. The patient was diagnosed as having pulmonary gas embolism caused by PVG. Objective: We consider PVG routes to pulmonary circulation, diagnosis of gas embolism caused by PVG, and treatment of gas embolism caused by PVG.Methods: We reviewed reports of eight cases of gas embolism caused by PVG and compared these cases to cases of gas embolism without PVG. Results: Mortality of gas embolism caused by PVG was 67%, positive blood culture was observed in six cases, and pulmonary edema was seen in three cases. PVG initially excites microbubble formation, which causes tissue damage in the liver and liver abscess. A large volume of PVG causes portal obstruction. As a result, portal hypertension, a portosystemic shunt or gastrointestinal congestion can occur. PVG can travel to the systemic vein through the liver or portosystemic shunt without anomaly and cause pulmonary gas embolism, followed by arterial embolism. In this environment, sepsis easily occurs. Echocardiography is useful for diagnosis of gas embolism caused by PVG, but the gas can be seen intermittently. The view of pulmonary edema is important for pulmonary gas embolism caused by PVG. Conclusion: It is important to treat the underlying disease, but PVG must be considered and treated as the gas embolism’s source.